Previous studies have demonstrated a cumulative effect of repeated ischemic insults in the gerbil. The present studies have been designed to address the potential role of the amino acid, glutamate, in this phenomenon, since glutamate is known to be released during ischemia and has been suggested to contribute to excitotoxic damage following ischemia and other insults. Extracellular glutamate was monitored in several brain regions by in vivo cerebral microdialysis. Current results demonstrate that a burst of glutamate release occurs during each ischemic insult, but that this appears to be cleared more rapidly than the larger increase seen after single longer occlusions. Further studies will attempt to determine whether the timing of glutamate release plays a critical role in the increased pathogy seen after repeated occlusions.